Diverse Contribution of Bone Marrow Cells to Neointimal Hyperplasia After Mechanical Vascular Injuries

Abstract— We and others have suggested that bone marrow-derived progenitor cells may contribute to the pathogenesis of vascular diseases. On the other hand, it was reported that bone marrow cells do not participate substantially in vascular remodeling in other experimental systems. In this study, three distinct types of mechanical vascular injuries were induced in the same mouse whose bone marrow had been reconstituted with that of GFP or LacZ mice. All injuries are known to cause smooth muscle cell (SMC) hyperplasia. At 4 weeks after wire-mediated endovascular injury, a significant number of the neointimal and medial cells derived from bone marrow. In contrast, marker-positive cells were seldom detected in the lesion induced by perivascular cuff replacement. There were only a few bone marrow-derived cells in the neointima after ligation of the common carotid artery. These results indicate that the origin of intimal cells is diverse and that contribution of bone marrow-derived cells to neointimal hyperplasia depends on the type of model.

[1]  U. Gröschel‐Stewart,et al.  Production of specific antibodies to contractile proteins, and their use in immunofluorescence microscopy , 1977, Histochemistry.

[2]  柏倉 祐司.  Isolation of bone marrow stromal cell-derived smooth muscle cells by a human SM22α promoter : In vitro differentiation of putative smooth muscle progenitor cells of bone marrow , 2004 .

[3]  H. Daida,et al.  Isolation of Bone Marrow Stromal Cell–Derived Smooth Muscle Cells by a Human SM22&agr; Promoter: In Vitro Differentiation of Putative Smooth Muscle Progenitor Cells of Bone Marrow , 2003, Circulation.

[4]  W. Edwards,et al.  Smooth muscle cells in human coronary atherosclerosis can originate from cells administered at marrow transplantation , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[5]  Mark M. Kockx,et al.  Phagocytosis and Macrophage Activation Associated With Hemorrhagic Microvessels in Human Atherosclerosis , 2003, Arteriosclerosis, thrombosis, and vascular biology.

[6]  A. Zalewski,et al.  Diverse Origin of Intimal Cells: Smooth Muscle Cells, Myofibroblasts, Fibroblasts, and Beyond? , 2002, Circulation research.

[7]  Qingbo Xu,et al.  Smooth Muscle Cells in Transplant Atherosclerotic Lesions Are Originated From Recipients, but Not Bone Marrow Progenitor Cells , 2002, Circulation.

[8]  I. Weissman,et al.  Little Evidence for Developmental Plasticity of Adult Hematopoietic Stem Cells , 2002, Science.

[9]  V. Fuster,et al.  Intimomedial Interface Damage and Adventitial Inflammation Is Increased Beneath Disrupted Atherosclerosis in the Aorta: Implications for Plaque Vulnerability , 2002, Circulation.

[10]  M. Makuuchi,et al.  Hematopoietic stem cells differentiate into vascular cells that participate in the pathogenesis of atherosclerosis , 2002, Nature Medicine.

[11]  A. Ruifrok,et al.  Hepatocytes and epithelial cells of donor origin in recipients of peripheral-blood stem cells. , 2002, The New England journal of medicine.

[12]  J. Hillebrands,et al.  Bone marrow does not contribute substantially to endothelial-cell replacement in transplant arteriosclerosis , 2002, Nature Medicine.

[13]  Julie H. Campbell,et al.  Neointimal Formation by Circulating Bone Marrow Cells , 2001, Annals of the New York Academy of Sciences.

[14]  S. M. Sims,et al.  Innate Diversity of Adult Human Arterial Smooth Muscle Cells: Cloning of Distinct Subtypes From the Internal Thoracic Artery , 2001, Circulation research.

[15]  Anthony Atala,et al.  Functional small-diameter neovessels created using endothelial progenitor cells expanded ex vivo , 2001, Nature Medicine.

[16]  W. Coleman,et al.  Adult-derived stem cells from the liver become myocytes in the heart in vivo. , 2001, The American journal of pathology.

[17]  P. Libby,et al.  Host bone-marrow cells are a source of donor intimal smooth- muscle–like cells in murine aortic transplant arteriopathy , 2001, Nature Medicine.

[18]  J. DiMaio,et al.  Adaptive Mechanisms That Preserve Cardiac Function in Mice Without Myoglobin , 2001, Circulation research.

[19]  M. Makuuchi,et al.  A mouse model of vascular injury that induces rapid onset of medial cell apoptosis followed by reproducible neointimal hyperplasia. , 2000, Journal of molecular and cellular cardiology.

[20]  K. Walsh,et al.  Fas ligand-deficient mice display enhanced leukocyte infiltration and intima hyperplasia in flow-restricted vessels. , 2000, Journal of molecular and cellular cardiology.

[21]  G. Ishii,et al.  Impairment of B lymphopoiesis in precocious aging (klotho) mice. , 2000, International immunology.

[22]  A. Becker,et al.  Neointimal tissue response at sites of coronary stenting in humans: macroscopic, histological, and immunohistochemical analyses. , 1998, Circulation.

[23]  R. Virmani,et al.  Interaction of genetic deficiency of endothelial nitric oxide, gender, and pregnancy in vascular response to injury in mice. , 1998, The Journal of clinical investigation.

[24]  V. Lindner,et al.  Remodeling and neointimal formation in the carotid artery of normal and P-selectin-deficient mice. , 1997, Circulation.

[25]  Amit Kumar,et al.  Remodeling with neointima formation in the mouse carotid artery after cessation of blood flow. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[26]  Tomoko Nakanishi,et al.  ‘Green mice’ as a source of ubiquitous green cells , 1997, FEBS letters.

[27]  L A Herzenberg,et al.  Disruption of overlapping transcripts in the ROSA beta geo 26 gene trap strain leads to widespread expression of beta-galactosidase in mouse embryos and hematopoietic cells. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[28]  P. Carmeliet,et al.  Vascular wound healing and neointima formation induced by perivascular electric injury in mice. , 1997, The American journal of pathology.

[29]  N. Maeda,et al.  Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. , 1992, Science.